Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury
Author(s) -
Changmeng Cui,
Jianzhong Cui,
Feng Jin,
Ying Cui,
Ran Li,
Xiaohua Jiang,
Yanxia Tian,
Richard C. Wang,
Pei Jiang,
Junling Gao
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000479571
Subject(s) - calcitriol , autophagy , neuroprotection , traumatic brain injury , calcitriol receptor , medicine , vitamin d and neurology , endocrinology , pharmacology , apoptosis , chemistry , biochemistry , psychiatry
Traumatic brain injury (TBI) is a major public health problem in the world and causes high rates of mortality and disability. Recent evidence suggests that vitamin D (VD) has neuroprotective actions and can promote function recovery after TBI. In vitro and in vivo studies have demonstrated that autophagy could be enhanced following supplementation with an active metabolite of VD (calcitriol). However, it is unclear whether autophagy participates in the protective effects of calcitriol after TBI. To test this hypothesis, we examined the protective effects of calcitriol on TBI-induced neurological impairment and further investigated whether calcitriol could modulate autophagy dysfunction-mediated cell death in the cortex region of rat brain.
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